Elevated Lp(a) independently predicts stenotic bioprosthetic valve degeneration, cohort of 174 (Eur Heart J Cardiovasc Imaging 2026)

Original title: Lipoprotein(a) and long-term structural valve degeneration of aortic bioprostheses

Eur Heart J Cardiovasc Imaging · 9 February 2026 · 7

Boute M, Salembier P, Pouleur AC, Pasquet A, Gerber BL, De Azevedo D, Gruson D, de Kerchove L, Kefer J, Beauloye C, Horman S, Maes F et al.

Cohort of 174 patients with bioprosthetic aortic valve replacement and available Lp(a), followed by echocardiography for a median 7.3 years (1372 studies), testing whether elevated Lp(a) predicts structural valve degeneration (SVD, VARC-3 criteria) and whether this differs by stenotic versus regurgitant phenotype. Over follow-up, 40 patients developed SVD (22 stenotic, 9 mixed, 9 regurgitant); 15-year cumulative incidence was 51%, median onset 14.8 years. Elevated Lp(a) (above 125 nmol/L) was associated with higher overall SVD risk (62% vs 47%, SHR 2.06, 95% CI 1.09-3.91) and specifically stenotic/mixed SVD (SHR 2.57, 95% CI 1.26-5.23), remaining independent after adjustment (adjusted SHR 3.00, 95% CI 1.48-6.07), with no association for regurgitant phenotypes (SHR 0.85, 95% CI 0.19-3.92). Each 25 nmol/L increase in Lp(a) conferred 13% higher risk in spline modelling. The authors propose Lp(a) as a biomarker of prosthetic valve vulnerability, supporting trials of Lp(a)-lowering therapy for valve durability.

Original abstract

Aims: Structural valve degeneration (SVD) is the leading cause of late bioprosthetic valve failure. Lipoprotein(a) [Lp(a)] contributes to native aortic valve calcification, but its role in SVD is unclear. We investigated whether elevated Lp(a) is associated with SVD after bioprosthetic aortic valve replacement (AVR) and whether this differs between stenotic and regurgitant phenotypes.

Methods And Results: We studied 174 bioprosthetic AVR patients with available Lp(a) levels over a median echocardiographic follow-up of 7.3 years (1372 studies). SVD was defined by VARC-3 criteria, and associations were analysed with Fine-Gray competing risk models. Lp(a) was evaluated categorically (≤ or > 125 nmol/L) and continuously using spline modelling. During follow-up, 40 patients developed SVD (22 stenotic, 9 mixed, and 9 regurgitant). The 15-year cumulative incidence was 51% with a median onset at 14.8 years. Elevated Lp(a) was associated with a higher risk of overall SVD (62% vs. 47%; SHR 2.06, 95% CI 1.09-3.91; P = 0.026) and specifically with stenotic/mixed phenotypes (SHR 2.57, 95% CI 1.26-5.23; P = 0.009). No association was observed with regurgitant phenotypes (SHR 0.85, 95% CI 0.19-3.92; P = 0.84). After multivariable adjustment, elevated Lp(a) remained an independent predictor of stenotic/mixed SVD (adjusted SHR 3.00, 95% CI 1.48-6.07; P = 0.002). Spline modelling showed a linear dose-response, with each 25 nmol/L increase in Lp(a) conferring 13% higher risk.

Conclusion: Elevated Lp(a) is independently associated with long-term risk of stenotic/mixed SVD. These findings highlight Lp(a) as a promising biomarker of prosthetic valve vulnerability and support investigation of emerging Lp(a)-lowering therapies to improve valve durability.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.